An impaired sense of smell is one of the earliest symptoms of Alzheimer’s, Parkinson’s, and some other neurodegenerative diseases. Could it be a useful diagnostic tool?
October 1, 2013|
Excerpt: Is it possible that the same pathological process is involved in the olfactory loss associated with most or all of these disorders, or is the olfactory system simply sensitive to damage from a range of disease-specific factors?
One hypothesis is that deficits in certain neurotransmitter systems are largely responsible for smell dysfunction that occurs in conjunction with neurodegenerative disease.
My Comment: In my mammalian model, the gonadotropin releasing hormone neuronal system and its effects on all other neurotransmitter systems in vertebrates links the epigenetic effects of nutrient stress and social stress to neurodegenerative diseases via what is already neuroscientifically known.
In this TS issue we read: “While there is little debate about the role pheromones play in eliciting insect reproductive behaviors, and general agreement about their role in certain mammals…” However, Doty is on record stating mammals do not have pheromones. “In this provocative book, renowned olfaction expert Richard L. Doty rejects this idea and states bluntly that, in contrast to insects, mammals do not have pheromones.” For contrast, see: Roles of sex and gonadal steroids in mammalian pheromonal communication.
“The claim that mammalian pheromones do not exist is an academically irresponsible misrepresentation. It is like saying that food odors do not exist for some species.” That fact becomes clear in the context of how dietary choline contributes to nutrient-dependent pheromone-controlled adaptive evolution of the human brain and behavior, and how the role of choline metabolism is directly linked to pheromone production in mice and in humans.
Doty writes here: “Cholinergic neurons that project from the basal forebrain to the olfactory bulb also directly modulate neural activity and inhibit the activity of cells critical for immune responses to brain damage and foreign agents, including microglia, astrocytes, and oligodendrocytes.” However, he just took the role of choline out of its context. Cholinergic neurons are not automagically involved in anything. All neuronal systems are adaptively evolved.
For example: In mice, coincident adaptive evolution involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes choline. The result of this synergy is (1) a liver enzyme that oxidizes trimethylamine to (2) an odor that causes (3) species-specific behaviors. Thus, the complex systems biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).
Returning to the proper context of choline in human aging and neurodegenerative diseases, the mouse model reveals that the aversive human body odor associated with fish odor syndrome can be epigenetically controlled by reducing dietary choline intake. It can also be controlled through antibiotic use. This is important in the context of chemical ecology and epigenetic effects of genetically predisposed nutrient-dependent pheromone-controlled human interactions, unless mice and humans are different types of mammals. Doty has inferred that we are different than other mammals, because humans do not produce nutrient-dependent species-specific pheromones via the conserved molecular mechanisms of every other species on the planet.
Doty short-circuits attempts to use what’s already neuroscientifically known from animal models of neurodegenerative diseases, which is that they are nutrient-dependent and pheromone-controlled via the epigenetic effects of nutrient stress and social stress. That’s why I said his claim is academically irresponsible. He eliminated from any further consideration whatsoever the likely role of glucose uptake and amino acid ingestion in the modulation of gonadotropin releasing hormone (GnRH), and the metabolism of nutrients to species-specific pheromones that modulate GnRH, and research on Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis.